Stroke is a prominent cause of serious, long-term disability and the third leading cause of death in the United States. Total health costs for disability due to stroke are estimated at 53.6 billion annually. Ischemic strokes comprise over 88% of all strokes, making them the most common type of cerebrovascular injury. Ischemic conditions in the brain cause neuronal death, leading to sensorimotor and cognitive deficits.
Research and development for the treatment of stroke therapies have until recently focused on approaches that would be utilized within the immediate 24 hours of stroke to either prevent or reduce neuronal cell damage (i.e., as a “neuroprotective agent” for “neuroprotection”). However, several decades of research have only yielded one approved acute stroke therapy by the United States Food and Drug Administration, thrombolysis with tissue plasminogen therapy (tPA). Moreover, the need to administer tPA within the first several hours after stroke, and other limitations, mean that the great majority of patients with an acute stroke do not receive this treatment. Otherwise, numerous pharmaceutical attempts at neuroprotection for stroke have failed in clinical trials (Grupke et al., Clinical Neurology and Neurosurgery, 129:1-9 (2015)). As a result, there is an increasing interest in developing therapies that are directed at promoting recovery during the period from the first several days to weeks and several months after stroke; a period during which many patients have some level of recovery, though many remain with residual disability (Hermann & Chopp, European Neurology, 72:317-325 (2014)). To date, no pharmaceutical agents have been successfully developed as a treatment to promote neurological recovery after stroke.